Transplantation into Genetically Alymphoid Mice as an Approach to Dissect the Roles of Uterine Natural Killer Cells during Pregnancy— A Review

Croy, B A; Santo, James P. Di; Greenwood, J.D.; Chantakru, Sirirak; Ashkar, Ali A.

doi:10.1053/plac.1999.0518

Cited by 33 publications

(30 citation statements)

References 19 publications

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“…Fetal liver cells (FLCs) were erythrocyte-depleted and two million FLCs were injected into the tail vein of sublethally irradiated (400 Rad, single dose) Rag-2 −/− Il2rg −/− immunodeficient recipient mice (Taconic emerging models program) [18]. Injections were performed within 4 hours of irradiation.…”

Section: Transplantation Into Immunodeficient Recipient Micementioning

confidence: 99%

“…5A and 5B). To determine whether this defect is cell-intrinsic, we transplanted wildtype or Sfpi1 BN/BN E.D.14.5 FLPs into sublethally irradiated immunodeficient mice lacking both Rag-2 and common gamma chain (Rag2 −/− Il2rg −/− mice) [18]. Whereas wild-type FLPs generated B cells efficiently in recipient mice six weeks after transplantation, Sfpi1 BN/BN FLPs failed to generate any detectable B lymphocytes in either spleen or bone marrow after six or nine weeks (Fig.…”

Section: B Cell Development Is Blocked In Sfpi1 Bn/bn Micementioning

confidence: 99%

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Reduction in PU.1 activity results in a block to B-cell development, abnormal myeloid proliferation, and neonatal lethality

Houston

Kamath

Schweitzer

et al. 2007

Experimental Hematology

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Objective-It has been demonstrated that high concentration of the transcription factor PU.1 (encoded by Sfpi1) promotes macrophage development, whereas low concentration induces B cell development in vitro. This has led to the hypothesis that lower levels of PU.1 activity are required for B cell than for macrophage development in vivo. We utilized an allele of Sfpi1 (termed BN) with a mutation in the first coding exon which resulted in a reduction of PU.1 expression in order to test this hypothesis. Methods-Using gene targeting in ES cells, two ATG-start site codons of PU.1 were mutated, resulting in reduced PU.1 expression originating from a third start codon. Mice were assayed for phenotypic abnormalities using fluorescence activated cell sorting, microscopy, and colony forming ability. In addition, isolated cells were tested for their differentiation potential in vitro and in vivo.Results-Lymphoid and myeloid cells derived from cultured Sfpi1 BN/BN fetal liver cells had reduced levels of PU.1 expression and activity. B cell development was intrinsically blocked in cells isolated from Sfpi1 BN/BN mice. In addition, myeloid development was impaired in Sfpi1 BN/BN fetal liver. However, neonatal Sfpi1 BN/BN mice had a dramatic expansion and infiltration of immature myeloid cells.Conclusion-Contrary to our original hypothesis, high levels of PU.1 activity are required to induce both myeloid and B cell development. In addition, neonatal mice homozygous for the hypomorphic allele acquire a myeloproliferative disorder and die within 1 month of age.

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Section: Transplantation Into Immunodeficient Recipient Micementioning

confidence: 99%

Section: B Cell Development Is Blocked In Sfpi1 Bn/bn Micementioning

confidence: 99%

Reduction in PU.1 activity results in a block to B-cell development, abnormal myeloid proliferation, and neonatal lethality

Houston

Kamath

Schweitzer

et al. 2007

Experimental Hematology

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“…Using mice lacking lymphocytes (RAG-2 −/− ), 3 uNK functions were identified as follows: 1) support of terminal decidual cell differentiation, 2) sensitization of spiral arteries resulting in pregnancy-associated dilation and elongation, and 3) formation of a transient lymphoid aggregates at the portal vessels and nerves serving as implantation sites [30] [31]. On the other hand, NK cell-deficient mice remained fertile and delivered normal numbers of viable pups, suggesting that NK cells may not be essential to healthy pregnancies in mice even though significant differences exist between the MLAp (mesometrial lymphoid aggregate of pregnancy) of NK cell-deficient mice and WT animals [32].…”

Section: Discussionmentioning

confidence: 99%

Elevated Birth Rates in CD62L (L-Selectin)-Deficient BALB/c Mice: Potential Involvement of NK Cells

Farkas¹,

Bódis²,

Mangold³

et al. 2014

OJI

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Background: L-selectin (CD62L) is a cell surface adhesion molecule recently shown to play a critical role in determining endometrial receptivity and implantation in humans. By contrast, the Lselectin ligand is missing from the rodent endometrium. Interestingly, CD62L (L-selectin)-deficient BALB/c mice delivered significantly higher numbers of viable offspring than wild type controls via mechanisms yet to be defined. Methods: Nulliparous CD62L-deficient (8 -10-week-old, n = 25) or wild type (n = 18) females were mated with 43 age-matched males. Animals were sacrificed at gestational day (GD) 9.5. Tissue samples were analyzed by immunostaining and flow cytometry. Results: Mating wild type and CD62L-deficient BALB/c mice revealed that the increased birth rate was due to the CD62L deficiency in females. Flow cytometric analysis demonstrated significant differences in the number of natural killer (NK) cells present in the uterus of pregnant CD62L-deficient mice compared to controls. Immunohistochemistry confirmed NK cell accumulation at the fetal-maternal interface. Discussion: Uterine NK cells have been shown to peak at GD 8 -10 at the fetal-maternal interface. NK cells might regulate mouse fertility rates by facilitating development of the maternal spiral arteries, thereby stimulating the formation of larger vessels that facilitate

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“…In mice, specialized terminally differentiated lymphocytes called uterine natural killer cells are primarily responsible for arterial remodeling in this species. 5,6 Trophoblastic invasion in mice is relatively shallow and is temporally restricted to late gestation, generally considered a minor contributor to arterial remodeling. In rats, invasion of trophoblast is more robust, extending deep into the myometrium in normal gestations.…”

Section: See Related Article Pp 1046-1054mentioning

confidence: 99%

Spiral Artery Remodeling in Preeclampsia Revisited

Burke

Karumanchi²

2013

Hypertension

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Transplantation into Genetically Alymphoid Mice as an Approach to Dissect the Roles of Uterine Natural Killer Cells during Pregnancy— A Review

Cited by 33 publications

References 19 publications

Reduction in PU.1 activity results in a block to B-cell development, abnormal myeloid proliferation, and neonatal lethality

Reduction in PU.1 activity results in a block to B-cell development, abnormal myeloid proliferation, and neonatal lethality

Elevated Birth Rates in CD62L (L-Selectin)-Deficient BALB/c Mice: Potential Involvement of NK Cells

Spiral Artery Remodeling in Preeclampsia Revisited

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